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Easter Flashcards

1
Q

What are the 4 steps in normal wound healing?

A
  1. Haemostasis
  2. Inflammation
  3. New tissue formation
  4. Tissue remodelling
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2
Q

What are the 5 steps in haemostasis and what is its effect?

A
  1. Release of collagen and von Willebrand factors
  2. Platelets adhere to collagen
  3. Release thromboxane
  4. Begin to aggregate together
  5. Bind to fibrinogen which is converted to a fibrin mesh
    = Platelet plug restoring physical barrier
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3
Q

What are the 5 steps in inflammation?

A
  1. Release of pro-inflammatory cytokines (prostaglandins, histamine and thromboxane)
  2. Increased permeability of vessels and recruitment of neutrophils
  3. Activation of complement and macrophages
  4. Macrophages stimulate angiogenesis and re-epithelialization
  5. T and B cells are recruited
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4
Q

What are the 5 steps in new tissue formation?

A
  1. Fibroblast migration and production of collagen
  2. Other epithelial cells are attracts
  3. Angiogenesis occurs due to VEGF
  4. Re-epithelialization by basal keratinocytes
  5. Reoganisation by collagenases and metalloproteinases
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5
Q

What 2 things occur in tissue remodelling?

A
  1. Collagen remodelling
    - Switch Type III for Type I which is stronger and has more cross-links
  2. Vascular maturation
    - Apoptosis of old vessels that are no longer required
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6
Q

How does Human Papilloma Virus (HPV) avoid the host immune system?

A
  1. Doesn’t express viral proteins until inflammation has decreased
  2. Rapid infection to avoid detection
  3. Infects reservoirs in basal cells
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7
Q

How does HPV evade the immune system, what proteins are involved?

A

E6
- Disrupts interferon signalling by interfering with Tyk2
E7
- Disrupts STAT signalling
- Suppresses Interferon response factor 1 (IRF1)
- Prevents presentation of antigen on MHC
E5
- Reduces conc of MHC

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8
Q

What are the pathological effects of the HPV proteins E6 and E7?

A

E6
- Suppresses p53, causes continuous cell cycling
- Inhibits differentiation by inhibiting NOTCH signalling
E7
- Binds to retinoblastoma, drives cell cycle

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9
Q

What are the two types of HPV?

A

Low risk
- Causes benign lesions
- Slight suppression of signalling
- e.g. HPV6, HPV11
High risk
- Causes lesions that can undergo neoplasia into cancer
- Aggressive suppression of signalling such as NOTCH
- e.g. HPV16, HPV18

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10
Q

What is NOTCH signalling? And what are its roles? (4)

A
  1. NOTCH receptor is transmembrane and can be bound to
  2. Binding causes release of intracellular domain
  3. Activates transcription and regulates expression
    Roles
    - Cell fate determination
    - Maintaining stem cell population
    - Regulates T cell development and differentiation
    - Involves in angiogenesis
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11
Q

How does the immune system persist with and eventually clear HPV infections?

A

Persistence
- due to low HPV gene expression levels
- E6 produces E-cadherin which reduces retention of Langerhan cells (DC) in the epithelium for detection
Clearance
- Activation of T cell immunity

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12
Q

Describe the vaccine against HPV

A
  • Recombinant vaccine
  • Mixed with an adjuvant
  • Mix of viral coat proteins
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13
Q

What are the steps in the pathology of Hepatitis B?

A
  1. Cytokines such as TNF-α and IL-6 are produced
  2. Activation of Nf-kB, causes resistance against apoptosis
  3. Production of ROS
  4. Chronic inflammation and tissue remodelling
    = Liver cirrhosis and Hepatocellular cancer
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14
Q

What are the steps in the pathology of H. pylori?

A
  1. Entry into the mucosal layer
  2. Secretion of mucinase, makes mucus less viscous
  3. Attach via BabA and BabB surface adhesins
  4. Secretes CagA pathogenicity island
    - Cells lose polarity and junctions disrupted
  5. VacA can be released causing pore formation
  6. Results in apoptosis
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15
Q

What is dysplasia and how is it different to carcinoma?

A

Dysplasia - changes in cell morphology. Doesn’t invade the basement membrane

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16
Q

What is immunosuppression?

A

When the host immune system activity is decreased

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17
Q

How do carcinomas and sarcomas differ?

A

Carcinoma - epithelial
Sarcoma - mesenchyme e.g. endothelial

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18
Q

What are the two differing types of immunosuppression?

A
  1. Congenital (genetic) v acquired
  2. Innate v adaptive
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19
Q

What treatments are the for autoimmunity?

A

NSAIDs (non-steroidal anti-inflammatory)
- Cell cycle inhibitors
- Anti-TNF e.g. infliximab
- Cyclosporin

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20
Q

What are the two ways in which immunosuppression can cause cancer?

A
  1. Lack of viral control
  2. Inability to respond to antigens, decreased MHC
21
Q

List 5 examples of immunosuppression-related cancers

A
  1. UV-induced cancers
  2. Merkel cell carcinoma
  3. Burkitt lymphoma
  4. Kaposi’s sarcoma
  5. HPV driven anogenital carcinoma
22
Q

How does UV-induced carcinoma develop?

A
  1. UV mutates keratinocyte DNA
  2. Causes increased production of IL-10
  3. IL-10 acts as an anti- inflammatory cytokine
23
Q

How does Merkel cell carcinoma develop?

A

Infection with merkel cell polyomavirus
- T region that becomes truncated can inhibit Rb and promote cell division

24
Q

How does HPV driven anogential carcinoma develop?

A
  • HPV infection releases E6 and E7
  • E6 and E7 target p53, Rb and NOTCH signalling, causing carcinoma
  • HPV only infects epithelial cells
  • Immunosuppressed patients, mainly develop cancers in the anogenital region
25
How does Burkitt lymphoma develop?
Infection with EBV (HHV-4 , a herpes virus) Targets B cells and leads to rapid proliferation Detection: Mib1 staining
26
What are the different variants of EBV and their effect on lymphoma development?
Endemic: Africa - Develop in the midline Sporadic + Immunocompromised related - Develop in the abdominal region
27
What is the cause for Kaposi's sarcoma?
HHV-8 (herpes) - Encodes LANA1 oncogene - Disrupts signalling (NOTCH, JAK/STAT) - Promotes anti-apoptosis - Disrupts Rb and p53
28
What are the 3 physical layers of defence in the foetus?
1. Placenta 2. Amniotic fluid - antimicrobial proteins 3. Cervical plug
29
What are the 4 sources of haematopoietic stem cells?
1. Yolk sac - Primitive wave 2. Aorta-gonad mesonephros 3. Liver 4. Bone marrow
30
What is the difference between primitive and definitive haematopoietis?
Primitive - only macrophages, RBC, megakaryocytes RBC- retain nuclei Definitive - all cells, RBC etc.
31
What prevents maternal and foetal cells from attacking each other upon recognition? Give an example of this response against maternal antigens.
Foetal DC or T cell cause development of Treg, instead of pro-inflammatory Evidence: Group with maternal antigens experienced a higher early rejection rate, mismatch with of maternal HLA antigen better than mismatch of paternal antigens from sibling - Burlingham et al., 1998
32
What are the properties of Treg cells? How are can these be identified?
FOXP3 and CD25 Analysed by flow cytometry
33
What are the 4 components of neonate immunology?
1. Arginase 2. Maternal IgG 3. Breast milk - IgA 4. Vaccination
34
What is the role arginase?
Breaks down L-arginine Molecule required by T cells to form TNF-α
35
How are maternal IgG transported across the placenta?
Presentation of FcRn Endocytosed and acidified - Occurs in second trimester e.g. against Bordetella pertussis
36
What are the components found in breast milk?
IgA - helps protect from GIT Lactoferrin- reduces iron, which bacteria require Lysosyme - antimicrobial, disrupting cell wall
37
Describe the pathology and treatment associated with Bordetella pertussis (Whooping cough)
Highly infectious Severe cough Treatment - Vaccination of mother, so that IgG are transferred
38
What is rhesus disease? How can it be treated?
- Caused when mother is Rh -ve and foetus is Rh +ve - Occurs when maternal and foetal blood mix during parturition - Injection of IgD, which will bind to foetal RBC and prevent detection
39
Why does susceptibility to different pathogens vary in the foetus ?
Different antibodies are transferred across with different levels of efficiency Measles - 100% SARS- Cov2 less efficient
40
What are developing therapies for genetic disease in utero?
1. In utero transplantation - Doesn't work against all diseases - Prevents excessive damage - Good against osteogenesis imperfecta, SCID 2. In utero gene therapy - extract and culture cells
41
What is the cause for SCID and what is its pathology?
Mutation in CD132 Cause lack of T and NK cells
42
Compare and contrast solid and liquid neoplasms
1. Invasiveness - Harder to tell in liquid cancers 2. Density dependent growth - Stromal cell not necessary in liquid cancers 3. Morphology - Benign and lymphoma similar looking in liquid cancers 4. Translocations - More translocations in haematopoietic cancers, due to VDJ recombination common for switching in chromosome 14
43
What are 5 steps in diagnosis of haematopoietic cancers?
1. Morphology inspection 2. Flow cytometry 3. Clonality studies 4. Molecular genetics 5. WHO classification
44
What is the difference between low and high grade lymphoma?
Low grade - smaller cells High grade - larger cells
45
What are the 3 key sites for the development of lymphoid neoplasia?
1. lymph nodes 2. Spleen/ thymus 3. Mucosal associated lymphoid tissue (MALT)
46
What are the 3 main causes of lymphoma?
1. Translocation driven - Follicular lymphoma chromosome 14 and 18 swap = Bcl-2 and CD10 presentation 2. Antigen driven - Antigen promotes translocation e.g. H.pylori activates Nf-kB 3. Point mutation driven - Rare, but single mutation can activate BRAF V600E in Hairy Cell Leukaemia
47
What are the 3 methods for immunotherapy?
1. Target checkpoint - Prevent checkpoint, cause constant activation of T cells via Ab against CTLA4 (Ipilimumab) and PD1/ PD-L1 2. Adoptive T cell therapies - Harvest T cells then reinfuse 3. Engineered adoptive T cells - CAR T cells, against CD19 on B cells
48
What is the role of RIG-I?
Cytoplasmic receptor detecting viral RNA and signals via Nf-kB and IRF3

Biology of Disease (4 decks)

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